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Am J Physiol Heart Circ Physiol 282: H547-H555, 2002; doi:10.1152/ajpheart.01019.2000
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Vol. 282, Issue 2, H547-H555, February 2002

Exacerbation of myocardial injury in transgenic mice overexpressing FGF-2 is T cell dependent

Johanna T. A. Meij1, Farah Sheikh1, Sarah K. Jimenez1, Peter W. Nickerson2, Elissavet Kardami3,4, and Peter A. Cattini1

Departments of 1 Physiology, 2 Internal Medicine and Immunology, and 3 Human Anatomy and Cell Science, University of Manitoba, Winnipeg R3E 3J7; and 4 Institute of Cardiovascular Sciences, St. Boniface Hospital Research Centre, Winnipeg, Manitoba, Canada R2H 2A6

Fibroblast growth factor-2 (FGF-2) is cardioprotective when added exogenously, stimulates cardiac myocyte proliferation, and is a mediator of tissue repair after injury. Furthermore, transgenic (TG) mice overexpressing FGF-2 in cardiac muscle demonstrate increased resistance to injury in an isolated heart model of ischemia-reperfusion. We investigated how increasing the endogenous FGF-2 levels in the heart affects the extent of myocardial damage induced by isoproterenol in vivo. Histopathological evaluation of hearts after intraperitoneal injection of isoproterenol yielded significantly higher scores for myocardial damage in FGF-2 TG lines compared with non-TG mice. After 1 day, FGF-2 TG mouse hearts displayed more cellular infiltration correlating with increased tissue damage. Immunostaining of non-TG and FGF-2 TG mouse hearts showed the presence of leukocytes in the infiltrate, including T cells expressing FGF receptor-1. Treatment of mice with T cell suppressors cyclosporin A and anti-CD3epsilon significantly decreased the level of myocardial injury observed after isoproterenol and equalized the histopathology scores in FGF-2 TG and non-TG hearts. These data demonstrate a direct T cell involvement in the response to isoproterenol-induced injury in vivo. Moreover, the findings indicate that the exacerbation of myocardial damage in FGF-2 TG mice was dependent on T cell infiltration, implicating FGF-2 in the inflammatory response seen in cardiac tissue after injury in vivo.

myocardium; lymphocytes


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